Show simple item record

dc.contributor.authorShahini, Negar
dc.contributor.authorMichelsen, Annika
dc.contributor.authorNilsson, Per
dc.contributor.authorEkholt, Karin
dc.contributor.authorGullestad, Lars
dc.contributor.authorBroch, Kaspar
dc.contributor.authorDahl, Christen Peder
dc.contributor.authorAukrust, Pål
dc.contributor.authorUeland, Thor
dc.contributor.authorMollnes, Tom Eirik
dc.contributor.authorYndestad, Arne
dc.contributor.authorLouwe, Maria Cornelia
dc.description.abstractThe complement system, an important arm of the innate immune system, is activated in heart failure (HF). We hypothesized that HF patients are characterized by an imbalance of alternative amplification loop components; including properdin and complement factor D and the alternative pathway inhibitor factor H. These components and the activation product, terminal complement complex (TCC), were measured in plasma from 188 HF patients and 67 age- and sex- matched healthy controls by enzyme immunoassay. Our main findings were: (i) Compared to controls, patients with HF had significantly increased levels of factor D and TCC, and decreased levels of properdin, particularly patients with advanced clinical disorder (i.e., NYHA functional class IV), (ii) Levels of factor D and properdin in HF patients were correlated with measures of systemic inflammation (i.e., C-reactive protein), neurohormonal deterioration (i.e., Nt-proBNP), cardiac function, and deteriorated diastolic function, (iii) Low levels of factor H and properdin were associated with adverse outcome in univariate analysis and for factor H, this was also seen in an adjusted model. Our results indicate that dysregulation of circulating components of the alternative pathway explain the increased degree of complement activation and is related to disease severity in HF patients.nb_NO
dc.publisherNature Publishing Groupnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleThe alternative complement pathway is dysregulated in patients with chronic heart failurenb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalScientific Reportsnb_NO
dc.description.localcode© 2017 The Authors. Published by Nature Publishing Group. This is an open access article licensed under a Creative Commons Attribution 4.0 International Licensenb_NO
cristin.unitnameInstitutt for klinisk og molekylær medisin

Files in this item


This item appears in the following Collection(s)

Show simple item record

Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal